Spatio-temporal motion correction and iterative reconstruction of in-utero fetal fMRI

Resting-state functional Magnetic Resonance Imaging (fMRI) is a powerful imaging technique for studying functional development of the brain in utero. However, unpredictable and excessive movement of fetuses have limited its clinical applicability. Previous studies have focused primarily on the accurate estimation of the motion parameters employing a single step 3D interpolation at each individual time frame to recover a motion-free 4D fMRI image. Using only information from a 3D spatial neighborhood neglects the temporal structure of fMRI and useful information from neighboring timepoints. Here, we propose a novel technique based on four dimensional iterative reconstruction of the motion scattered fMRI slices. Quantitative evaluation of the proposed method on a cohort of real clinical fetal fMRI data indicates improvement of reconstruction quality compared to the conventional 3D interpolation approaches.Comment: Accepted by MICCAI 202

An ode to fetal, infant, and toddler neuroimaging: chronicling early clinical to research applications with MRI, and an introduction to an academic society connecting the field

Fetal, infant, and toddler neuroimaging is commonly thought of as a development of modern times (last two decades). Yet, this field mobilized shortly after the discovery and implementation of MRI technology. Here, we provide a review of the parallel advancements in the fields of fetal, infant, and toddler neuroimaging, noting the shifts from clinical to research use, and the ongoing challenges in this fast-growing field. We chronicle the pioneering science of fetal, infant, and toddler neuroimaging, highlighting the early studies that set the stage for modern advances in imaging during this developmental period, and the large-scale multi-site efforts which ultimately led to the explosion of interest in the field today. Lastly, we consider the growing pains of the community and the need for an academic society that bridges expertise in developmental neuroscience, clinical science, as well as computational and biomedical engineering, to ensure special consideration of the vulnerable mother-offspring dyad (especially during pregnancy), data quality, and image processing tools that are created, rather than adapted, for the young brain.UL1 TR001863 - NCATS NIH HHS; R01 MH117983 - NIMH NIH HHS; K24 MH127381 - NIMH NIH HHS; UL1 TR001873 - NCATS NIH HHS; TL1 TR001875 - NCATS NIH HHS; T32 MH018268 - NIMH NIH HHS; ZIA MH002782 - Intramural NIH HHS; UL1 TR003015 - NCATS NIH HHS; KL2 TR003016 - NCATS NIH HHS; R01 HD065762 - NICHD NIH HHS; R03 EB022754 - NIBIB NIH HHS; R21 HD095338 - NICHD NIH HHS; R01 HD093578 - NICHD NIH HHS; R01 HD099846 - NICHD NIH HHS; R01 HD100560 - NICHD NIH HHSPublished versio

Cortisol, cognition and the ageing prefrontal cortex

The structural and functional decline of the ageing human brain varies by brain region, cognitive function and individual. The underlying biological mechanisms are poorly understood. One potentially important mechanism is exposure to glucocorticoids (GCs; cortisol in humans); GC production is increasingly varied with age in humans, and chronic exposure to high levels is hypothesised to result in cognitive decline via cerebral remodelling. However, studies of GC exposure in humans are scarce and methodological differences confound cross-study comparison. Furthermore, there has been little focus on the effects of GCs on the frontal lobes and key white matter tracts in the ageing brain. This thesis therefore examines relationships among cortisol levels, structural brain measures and cognitive performance in 90 healthy, elderly community-dwelling males from the Lothian Birth Cohort 1936. Salivary cortisol samples characterised diurnal (morning and evening) and reactive profiles (before and after a cognitive test battery). Structural variables comprised Diffusion Tensor Imaging measures of major brain tracts and a novel manual parcellation method for the frontal lobes. The latter was based on a systematic review of current manual methods in the context of putative function and cytoarchitecture. Manual frontal lobe brain parcellation conferred greater spatial and volumetric accuracy when compared to both single- and multi-atlas parcellation at the lobar level. Cognitive ability was assessed via tests of general cognitive ability, and neuropsychological tests thought to show differential sensitivity to the integrity of frontal lobe sub-regions. The majority of, but not all frontal lobe test scores shared considerable overlap with general cognitive ability, and cognitive scores correlated most consistently with the volumes of the anterior cingulate. This is discussed in light of the diverse connective profile of the cingulate and a need to integrate information over more diffuse cognitive networks according to proposed de-differentiation or compensation in ageing. Individuals with higher morning, evening or pre-test cortisol levels showed consistently negative relationships with specific regional volumes and tract integrity. Participants whose cortisol levels increased between the start and end of cognitive testing showed selectively larger regional volumes and lower tract diffusivity (correlation magnitudes <.44). The significant relationships between cortisol levels and cognition indicated that flatter diurnal slopes or higher pre-test levels related to poorer test performance. In contrast, higher levels in the morning generally correlated with better scores (correlation magnitudes <.25). Interpretation of all findings was moderated by sensitivity to type I error, given the large number of comparisons conducted. Though there were limited candidates for mediation analysis, cortisol-function relationships were partially mediated by tract integrity (but not sub-regional frontal volumes) for memory and post-error slowing. This thesis offers a novel perspective on the complex interplay among glucocorticoids, cognition and the structure of the ageing brain. The findings suggest some role for cortisol exposure in determining age-related decline in complex cognition, mediated via brain structure